Congenital pneumonia is an important cause of premature labor and perinatal death. Although alveolar macrophages (AMs) are the primary defense against infected, inhaled amniotic fluid, perinatal factors which affect macrophage physiology have been incompletely studied. Glucocorticoids alter antibody receptor on mononuclear phagocytes, and our recent investigations have shown that antibody-coated Group B streptococci (GBS) are required to stimulate cell receptors and initiate oxidative metabolism by newborn and maternal AMs. Based on these relationships, we will study the following factors and their effect on AM function: 1) antenatal glucocorticoid therapy, 2) transplacental anti-GBS antibody, 3) perinatal age and oxidative metabolism and 4) steroids, perinatal age, and immune cell receptors. Oxidative metabolism of perinatal rabbit AMs will be ascertained by O2 production (spectrophotometric measurement of cytochrome C reduction plus/minus SOD) and O2 consumption (measured polaragraphically with a Clark electrode) following cellular stimulation with particulate-opsonin complexes. Simultaneously prepared monolayers of AMs will quantitate Fc and C3b receptors by EA and EAC rosetting and ingestion. The role of transplacentally acquired antibody will be studied following GBS aerosol infection of perinatal rabbits whose mothers are unimmunized or hyperimmunized against GBS. In vivo ingestion (histologic localization of 100 intra- or extracellular GBS in the fixed right lung) and bacterial clearance (serial colony counts of the homogenized left lung) rates are ascertained after aerosol infection and correlated with histologic evidence of intracellular fluorscent IgG-GBS complexes. Serologic titers of individual animals are also compared with bacterial ingestion and clearance rates. Steroid-treated and control rabbit litters will be simultaneously infected with aerosols of Staphylococcus aureus, and in vivo rates of ingestion and killing determined. These in vivo findings will be contrasted with measurements of the numbers of Fc receptors and the oxidative metabolism of steroid-treated perinatal AMs. This study concurs with our long-term objective concerning the characterization of newborn lung macrophage physiology and its role in the pathogenesis of congenital pneumonia. Information derived from this research should enhance our care of human newborns and the prevention of premature delivery.